As one of the most common malignant tumors， digestive system tumors exhibit an increase in the incidence and mortality year by year. Its pathogenesis is complex， making it difficult to carry out early prevention. Autophagy is a process in which cells use lysosomes to degrade their organelles and macromolecules to maintain cellular homeostasis under the regulation of autophagy-related genes. Cellular autophagy has a dual regulatory effect on the tumor microenvironment， which always affects the occurrence and development of digestive system tumors. Therefore， the effect and mechanism of action of cellular autophagy on digestive system tumors have become a hot topic in tumor therapy in recent years. Meanwhile， the remarkable research results of targeted autophagy drugs indicate that cellular autophagy may become an important target for anti-digestive system tumors. Traditional Chinese medicine （TCM） has been widely used in the comprehensive treatment of digestive system tumors with good efficacy. A variety of active ingredients in TCM， such as flavonoids， glycosides， terpenoids， quinones， and alkaloids， can increase the expression of autophagy-associated proteins microtubule-associated protein 1 light chain 3 （LC3）Ⅱ/Ⅰ， autophagy-related gene （ATG）5， ATG7， inhibit the expression of autophagy-related protein p62 ， and induce autophagy in digestive system tumor cells， thereby exerting the anti-digestive system tumor effect. By summarizing the research results in recent years on the modulation of cell autophagy by active ingredients in TCM to fight against digestive system tumors， this paper analyzed the relevant signaling pathways， regulatory factors， and functional characteristics of cell autophagy modulation， so as to elucidate the mechanism by which active ingredients of TCM induce autophagy and to provide ideas and references for clinical application.

As one of the most common malignant tumors， digestive system tumors exhibit an increase in the incidence and mortality year by year. Its pathogenesis is complex， making it difficult to carry out early prevention. Autophagy is a process in which cells use lysosomes to degrade their organelles and macromolecules to maintain cellular homeostasis under the regulation of autophagy-related genes. Cellular autophagy has a dual regulatory effect on the tumor microenvironment， which always affects the occurrence and development of digestive system tumors. Therefore， the effect and mechanism of action of cellular autophagy on digestive system tumors have become a hot topic in tumor therapy in recent years. Meanwhile， the remarkable research results of targeted autophagy drugs indicate that cellular autophagy may become an important target for anti-digestive system tumors. Traditional Chinese medicine （TCM） has been widely used in the comprehensive treatment of digestive system tumors with good efficacy. A variety of active ingredients in TCM， such as flavonoids， glycosides， terpenoids， quinones， and alkaloids， can increase the expression of autophagy-associated proteins microtubule-associated protein 1 light chain 3 （LC3）Ⅱ/Ⅰ， autophagy-related gene （ATG）5， ATG7， inhibit the expression of autophagy-related protein p62 ， and induce autophagy in digestive system tumor cells， thereby exerting the anti-digestive system tumor effect. By summarizing the research results in recent years on the modulation of cell autophagy by active ingredients in TCM to fight against digestive system tumors， this paper analyzed the relevant signaling pathways， regulatory factors， and functional characteristics of cell autophagy modulation， so as to elucidate the mechanism by which active ingredients of TCM induce autophagy and to provide ideas and references for clinical application.

Background Lung cancer, one of the most common malignant tumors worldwide, has long ranked first in cancer incidence and mortality, posing a severe challenge to public health systems. Objective To analyze the trends in incidence, mortality, and disability-adjusted life years (DALYs) of lung cancer among residents in Jing'an District, Shanghai, from 2002 to 2021, explore the impacts of population aging, population growth, and age-specific prevalence on disease burden, and provide a scientific basis for optimizing regional lung cancer prevention and control strategies. Methods Based on the cancer registration and cause-of-death surveillance data of registered residents in Jing'an District, Shanghai, from 2002 to 2021, Joinpoint regression models were used to analyze the annual change trends (APC) and average annual change trends (AAPC) of lung cancer incidence, mortality, DALY rate, and their age-standardized rates. Decomposition analysis was applied to quantify the contribution of population aging, population growth, and age-specific prevalence to changes in the number of new cases, deaths, and DALYs. Results From 2002 to 2021, the crude incidence rate of lung cancer in Jing'an District increased from 68.00 per 100000 to 144.36 per 100000 (AAPC=4.86%, P<0.001), and the age-standardized incidence rate rose from 43.09 per 100000 to 61.46 per 100000 (AAPC=2.89%, P<0.001). The growth rate of incidence was significantly higher in females (AAPC=6.73%) than in males (AAPC=3.62%). The crude mortality rate increased from 58.08 per 100000 to 66.11 per 100000 (AAPC=1.10%, P<0.001), while the age-standardized mortality rate decreased (AAPC=−1.54%, P<0.001). The crude DALY rate showed an upward trend (AAPC=0.94%, P=0.002), whereas the age-standardized DALY rate declined (AAPC=−1.63%, P<0.001). Significant differences were observed across genders and age groups: the mortality and DALY rates increased in males aged 60-64 years, while the fastest incidence growth occurred in females aged 45-64 years. The results of decomposition analysis indicated that the increase in new cases was primarily attributed to age-specific incidence (38.15%) and aging (37.31%); the growth in deaths and DALYs was driven by aging, while age-specific mortality and population growth showed offsetting effects. From 2002 to 2021, the probability of premature death from lung cancer among males (2.04%-2.52%) in Jing'an District showed no statistically significant trend (AAPC=−0.28%, P=0.440), while it presented a decreasing trend in the total population (1.37%-1.89%) and females (0.72%-1.26%) (AAPC=−0.80% and −2.23%, respectively; P=0.029 and <0.001, respectively). Conclusion From 2002 to 2021, the risk of lung cancer incidence in Jing’an District, Shanghai, continue to increase, with a disease burden exhibiting significant heterogeneity by gender and age: key features include a rapid increase in new cases and a trend toward younger onset among females, alongside rising mortality risk among males aged 60–64 years. Population aging and increasing age-specific incidence rates are primary drivers of the growing number of cases, while declining age-specific mortality rates mitigate the rise in mortality burden.

ObjectiveTo investigate the therapeutic effect of Astragali Radix-mediated changes in gut microbiota on treating type 2 diabetes （T2DM）. MethodsA 12-week randomized， placebo-controlled clinical trial enrolled eighty patients with newly diagnosed type 2 diabetes and poor glycemic control in the Qi deficiency type. All patients received insulin therapy. The observation group （40 cases） was administered with Astragali Radix Granules， while the control group （40 cases） received a placebo. Both treamtents were taken orally twice daily. Changes in gut microbiota were assessed by 16s rDNA sequencing. Serum glucagon-like peptide-1 （GLP-1） levels were measured using enzyme-linked immunosorbent assay （ELISA）. Glucose metabolism indicators including fasting blood glucose （FPG）， 2-hour postprandial blood glucose （2 h PG），glycated albumin（GA）， and glycated hemoglobin （HbA1c） were evaluated. Pancreatic function was evaluated using fasting C-peptide （FCP）， 2-hour postprandial C-peptide （2 h CP）， and C-peptide area under the curve （AUC_cp）. Traditional Chinese medicine （TCM） syndrome scores， clinical efficacy， and safety indicators were also observed. ResultsIn terms of glucose metabolism indicators， compared with the baseline， both groups exhibited significantly lower FPG， 2 h PG， GA and HbA1C （P<0.01），while FCP， 2 h CP and AUC_cp were significantly higher （P<0.01）. Compared with the control group after the treatment， the observation group showed significantly lower FPG， 2 h PG， GA and HbA1C（P<0.05， P<0.01），and significantly higher FCP， 2 h CP and AUC_cp （P<0.05， P<0.01）， indicating that Astragali Radix can improve glucose metabolism. In terms of the diversity of gut microbiota， no significant differences were detected in the Chao1， Shannon and Simpson indexes of the two groups compared with their respective baselines. However， compared with the post-treatment control group， the observation group demonstrated significant increases in the Chao1， Shannon and Simpson indexes （P<0.05， P<0.01）. The β-diversity analysis showed significant separation in gut microbiota composition before and after treatment in both groups， indicating that Astragali Radix can significantly alter the structure and improve the diversity of gut microbiota. At the phylum level， compared with the baseline， both groups showed a significant increase in the relative abundance of Bacteroidota（P<0.01）. The relative abundance of the potentially harmful phylum Proteobacteria was significantly lower in the observation Group after treatment （P<0.01）. Compared with the post-treatment control group， the observation group had a significantly higher relative abundance of Bacteroidota（P<0.01）. No significant difference was found in Firmicutes/Bacteroidota （F/B） ratio between the two groups after treatment， and other phyla showed no significant differences. At the genus level， compared with the baseline， the observation group exhibited a significant increase in Bacteroides （P<0.01） and a significant decrease in Escherichia-Shigella （P<0.01）， whereas no significant difference was seen in the control group . Compared with the control group after treatment， the observation group after treatment had a significantly higher relative abundance of Bacteroides （P<0.01）. No significant differences were seen in other genera. Linear discriminant analysis （LDA） identified potential characteristics taxa： in the observation group， Bacteroidota at the phylum level and Bacteroides and Dubosiella at the genus level， in the control group， Proteobacteria at the phylum level as well as Barnesiella and Staphylococcus at the genus level. Correlation analysis based on a heatmap revealed that GLP-1 levels were positively correlated with Firmicutes， F/B ratio and Fusobacterium， and negatively correlated with Bacteroidota， Proteobacteria， Bacteroides and Escherichia-Shigella. In terms of clinical efficacy， compared with the control group， the total effective rate of the observation group was significantly higher （P<0.05）. Compared with the baseline， the scores for shortness of breath， fatigue， weakness， spontaneous sweating and reluctance to speak significantly decreased in both groups （P<0.01）. Compared with the control group after treatment， the score for weakness was significantly lower in the observation group （P<0.01），indicating that Astragali Radix could improve clinical symptoms and alleviate weakness symptoms. In terms of safety， compared with the baseline， alanine aminotransferase （ALT） levels significantly decreased in both groups （P<0.05，P<0.01），indicating that Astragali Radix did not induce any significant abnormalities in liver and kidney functions. ConclusionAstragali Radix demonstrates the potential to significantly improve the gut microbiota environment in patients of newly diagnosed type 2 diabetes with Qi deficiency. The therapeutic effect may contribute to glycemic control， possibly mediated by an elevation in GLP-1 level. These findings may support its further clinical investigations and potential applications.

Hepatocellular carcinoma （HCC）， a malignancy with high mortality， exhibits poor survival rates and prognosis. The profound suppression of the tumor immune microenvironment （TIME） and the abnormal hyperactivity of metabolic reprogramming （MR） are the two primary factors driving HCC progression. Traditional Chinese medicine has demonstrated significant efficacy in HCC treatment. The team proposed that "deficiency of healthy Qi and stasis toxins" was the core pathogenesis of HCC， closely associated with TIME suppression and MR hyperactivity. This paper proposed that a suppressed state of the TIME was the biological manifestation of "deficiency of healthy Qi"， where the functional exhaustion of effector T lymphocytes and natural killer cells reflected the decline of "healthy Qi" in eliminating pathogens. Conversely， the expansion and activation of immunosuppressive cells， such as regulatory T cells （Tregs）， M2-like tumor-associated macrophages （TAM-M2）， and myeloid-derived suppressor cells （MDSCs） ， represent the dysfunction of "healthy Qi" in maintaining homeostasis. MR serves as the material basis of "stasis toxins". Stasis toxins exhibit heat stagnation， manifested by abnormal hyperactivity of glycolysis and lipid synthesis. They demonstrate migratory propensity， as toxic metabolites like lactic acid and prostaglandin E2 promote tumor invasion and metastasis. They display a consumptive nature， reflected in the functional suppression of immune cells. The vicious cycle between TIME and MR is the biopathological reflection of "deficiency of healthy Qi intertwined with stasis toxins". Immunosuppression exacerbates MR， while toxic metabolites further impair immune function， establishing a pathogenic chain of "deficiency leading to stasis， and stasis toxins damaging healthy Qi". The primary therapeutic approach is reinforcing healthy Qi， resolving stasis， and removing toxins， which can reinforce and tonify healthy Qi to regulate pathways， such as phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt）， C-X-C chemokine receptor type 4/ C-X-C chemokine ligand 12 （CXCR4/CXCL12）， and toll-like receptor 4/ nuclear factor-kappa B/ signal transducer and activator of transcription 3 （TLR4/NF-κB/STAT3）， adjust T lymphocyte ratios， inhibit Tregs/TAM-M2 function， and downregulate immune checkpoints， including programmed death ligand 1/programmed death 1（PD-L1/PD-1）， and reshape TIME. It is also involved in resolving stasis and removing toxins to modulate phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin （PI3K/Akt/mTOR） and hypoxia-inducible factor-1α （HIF-1α） signaling pathways， suppress key enzymes in glycolysis and lipid synthesis， and block toxic metabolite production. Thus， this therapy synergistically regulates the immune and metabolic network， breaks the vicious cycle of "deficiency in healthy Qi and stasis toxins"， and offers a novel strategy for integrating traditional Chinese medicine and Western medicine in HCC treatment.

Chronic heart failure （CHF） is the final stage of cardiovascular diseases. It is a complex syndrome， with dyspnea and edema as the main clinical manifestations， and it is characterized by complex disease conditions， difficult cure， and high mortality. Ferroptosis， a new type of programmed cell death， is different from other types of programmed cell death. Ferroptosis is iron-dependent， accompanied by lipid peroxide accumulation and mitochondrial shrinkage， becoming a hot research topic. Studies have confirmed that ferroptosis plays a key role in the occurrence and development of CHF. The regulation of ferroptosis may become a potential target for the treatment of CHF in the future. The theory of Qi deficiency and stagnation refers to the pathological state of original Qi deficiency and abnormal transportation and distribution of Qi， blood， and body fluid， which has guiding significance for revealing the pathogenesis evolution of some chronic diseases. We believe that Qi deficiency and stagnation is a summary of the pathogenesis of ferroptosis in CHF. Deficiency of Qi （heart Qi） is the root cause of CHF， and stagnation （phlegm turbidity and blood stasis） is the branch of this disease. The two influence each other in a vicious circle to promote the development of this disease. Traditional Chinese medicine （TCM） plays an important role in the treatment of CHF， improving the prognosis and quality of life of CHF patients. This paper explores the correlation between the theory of Qi deficiency and stagnation and the mechanism of ferroptosis in CHF. Furthermore， this paper reviews the mechanism of Chinese medicines and compound prescriptions in preventing and treating CHF by regulating ferroptosis according to the principles of replenishing Qi and dredging to remove stagnation， aiming to provide new ideas and methods for the treatment of CHF with TCM.

BACKGROUND:In the preparation of injectable extracellular matrix materials,most of the materials require pepsin digestion followed by combination with other matrix components like hydrogels for pulp tissue regeneration,which also means the destruction of the microenvironment retained by natural extracellular matrix materials.OBJECTIVE:To investigate the effect of injectable dental pulp extracellular matrix prepared by grinding treatment on the regeneration of dental pulp tissue.METHODS:(1)The dental pulp tissue from pig teeth was prepared into acellular dental pulp matrix materials after acellular treatment.After freezing in liquid nitrogen and high-speed grinding,the injectable dental pulp extracellular matrix was prepared.Then,the differences in cell adhesion efficiency and microstructure between the injectable dental pulp extracellular matrix and natural dental pulp extracellular matrix were compared.Immunohistochemical analysis was used to analyze extracellular matrix protein components in injectable dental pulp extracellular matrix.(2)Injectable dental pulp extracellular matrix material inoculated with dental pulp stem cells was injected into the dental pulp cavity constructed from the dentin matrix material.The samples were obtained after 1,3,and 5 weeks of subcutaneous implantation in nude mice to observe the in vivo conversion rate of injectable dental pulp extracellular matrix materials and the regeneration ability of ectopic dental pulp tissue under the skin of nude mice.RESULTS AND CONCLUSION:(1)Compared with the dental pulp extracellular matrix,the injectable dental pulp extracellular matrix significantly improved the cell adhesion rate and retained the porous collagen structure similar to that of natural dental pulp extracellular matrix.(2)Compared with the natural dental pulp extracellular matrix,immunohistochemical staining showed that there was no significant difference in the expression of fibronectin,collagen type Ⅰ,and integrin β1 in the injectable dental pulp extracellular matrix,while the expression of fibronectin was significantly decreased.(3)In vivo experiments show that the injectable dental pulp extracellular matrix has excellent angiogenesis ability and promotes the formation of pulp-like tissues.The results exhibit that the milled injectable dental pulp extracellular matrix can still be used as an effective scaffold for the regeneration of dental pulp.

Objective To construct a machine learning prediction model for diabetic kidney disease(DKD)in type 2 diabetes mellitus(T2DM)patients in the plain-sand and loess hilly areas of Gansu Province,and analyze the interpretability of the model.Methods A multi-stage stratified random sampling method was used to collect the data of T2DM patients in the two areas.After key feature screening,eight ML prediction models were constructed for the risk of DKD in the two areas.The receiver operating characteristic(ROC)curve,accuracy and F1 index were used to evaluate the model,and Shapley additive explanation(SHAP)algorithm was used for model interpretation.Results A total of 1599 patients with T2DM were enrolled in this study.After feature screening,ten variables were selected for model construction in the plain-sand areas.Among the eight models,the gradient boosting decision tree(GBDT)model had the highest prediction efficiency.The area under the curve(AUC)of the test dataset was 0.972,the accuracy was 0.949,and the F1 index was 0.884.In the loess hilly region,12 variables were included in the model,and the best model was the random forest(RF).The AUC of the test set was 0.966,the accuracy was 0.951,and the F1 index was 0.861.SHAP analysis showed that in addition to serum creatinine,age,LDL-C,HbA1c,DM duration,serum uric acid and urinary microalbumin were also closely related to the high risk of DKD.Conclusions The GBDT and RF models have good predictive efficiency for the occurrence of DKD in the two areas,which can be used for the screening of DKD high-risk populations and the in-depth exploration of potential risk factors in the two areas.

Objective:To investigate the curative effect of hemodialysis combined with hemoperfusion in treating chronic renal failure and the effect of that on the expression level of serum inflammatory cytokine of patients.Methods:A total of 100 patients with chronic renal failure who admitted to the First Affiliated Hospital of Xinjiang Medical University from January 2021 to June 2023 were selected,and they were divided into control group(50 cases who received with hemodialysis treatment)and study group(50 cases who received hemodialysis combined with hemoperfusion)according to different treatment methods of blood purification.The overall efficiency rates of the treatment of two groups were compared.The expression levels of pro-inflammatory cytokines[interleukin-6(IL-6)and interleukin-17(IL-17)]and the interleukin-10(IL-10)of anti-inflammatory cytokine,as well as β2-microglobulin(β2-MG),parathyroid hormone(PTH)and serum CD16,were monitored before and after treatment.The incidence rate of adverse reaction at the end of treatment was also recorded.Results:The overall efficiency rates of the treatment of control group and study group were 84.00%and 96.00%,and the overall efficiency rate of study group was significantly higher than that of control group(x2=4.000,P<0.05).After treatment,both groups showed decrease in pro-inflammatory cytokines(IL-6 and IL-17),and increase in anti-inflammatory cytokine(IL-10).The IL-6 and IL-17 levels of study group were lower than those of control group,and the IL-10 level of study group was higher than that of control group,and the differences of them between two groups were significant(t=8.835,4.138,9.196,P<0.05),respectively.Compared with β2-MG,PTH and CD16 after treatment in control group,the β2-MG and PTH levels in study group were lower,and the CD16 level of study group was higher,and the differences of them between two groups were significant(t=10.076,15.336,2.050,P<0.05),respectively.The overall incidence rates of adverse reaction of control group and study group were respectively 18.00%and 4.00%,and the overall incidence rate of adverse reaction of study group was significantly lower than that of control group,with statistically significant difference(x2=4.000,P<0.05).Conclusion:The treatment of hemodialysis combined with hemoperfusion can improve the curative efficiency for patients with chronic renal failure,and inhibit the levels of serum pro-inflammatory cytokines and macromolecules(β2-MG and PTH),and regulate the levels of anti-inflammatory cytokines and CD16,and reduce the incidence of adverse reaction.

Objective:To analyze the clinical efficacy of vascular resection and reconstruction during radical resection in patients with hilar cholangiocarcinoma.Methods:A retrospective analysis was conducted on the clinical data of 151 patients with hilar cholangiocarcinoma who underwent radical resection in the Department of Hepatobiliary and Pancreatic Surgery at the First Affiliated Hospital of Anhui Medical University from April 2018 to April 2025. Among them, there were 91 males and 60 females, with an age of (65.4±10.5) years. According to whether radical resection of hilar cholangiocarcinoma was combined with vascular resection, the patients were divided into the vascular resection group ( n=19) and the control group ( n=132). Postoperative complications such as bleeding, biliary fistula, and thrombosis were recorded, along with intraoperative blood loss, R 0 resection rate, perioperative mortality, and recurrence rate at six months postoperatively. Results:The preoperative bilirubin reduction and intraoperative blood loss in the vascular resection group were 6 (31.6) and 200 (200, 200) ml, respectively, while those in the control group were 45 (34.1) and 200 (100, 200) ml, respectively. There were no statistically significant differences between the two groups (all P>0.05). The combined liver resection, Billroth operation type Ⅰ-Ⅱ, and operation time in the vascular resection group were 18 (94.7), 1 (5.3), and 420 (377.5, 512.5) min, respectively, while those in the control group were 79 (59.8), 38 (28.8), and 322.5 (260, 410) min, respectively. There were statistically significant differences between the two groups (all P<0.05). The R 0 resection, perioperative mortality rate, postoperative bleeding, postoperative biliary fistula, postoperative thrombosis, postoperative pathology (adenocarcinoma), and recurrence rate at 6 months after surgery in the vascular resection group were 16 (84.2), 2 (10.5), 2 (10.5), 3 (15.8), 1 (5.3), 18 (94.7), and 1 (5.9), respectively, while those in the control group were 103 (78.0), 5 (3.8), 5 (3.8), 25 (18.9), 2 (1.5), 121 (91.7), and 6 (4.7), respectively. There were no statistically significant differences between the two groups (all P>0.05). The postoperative hospital stay, alanine aminotransferase on the 1st and 3rd day after surgery, and postoperative liver failure in the vascular resection group were 18 (13.5, 21.5) days, 619 (305.4, 1 634.0) U/L, and 1 (5.3), respectively, while those in the control group were 14 (11, 18), 254.5 (139.3, 468.3) U/L, and 3 (2.3), respectively. There were statistically significant differences between the two groups (all P<0.05). Conclusion:Vascular resection and reconstruction during radical resection of hilar cholangiocarcinoma in patients has certain safety and efficacy.